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NEU2 > Infectious disease > Flashcards

Infectious disease Flashcards

Bacteriology, virology

1
Q

What are the 3 potential routes of infection affecting the nervous system?

A
  • Direct extension e.g. from otitis interna or sinusitis
  • Bacterial embolisation within the brain
  • Bacterial penetration through BBB
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2
Q

List the potential causes of meningitis, encephalitis and meningoencephalitis

A
  • Bacteria
  • viruses
  • fungi
  • Protozoa
  • Rickettsia
  • Parasite migrations
  • Chemical agents
  • Idiopathic or immune mediated diseases
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3
Q

List the ways in which pathology of the nervous system can occur

A
  • Invasion of neuronal tissue by pathogenic agent
  • Induction of an immune response
  • Toxin or drug getting into and interacting with the nervous system
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4
Q

How may a pathogenic agent invade the neuron tissue?

A
  • Direct invasion of peripheral nerves
  • From adjacent structures such as the meninges
  • From blood (haematogenous)
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5
Q

Explain how an immune response can cause pathology of the nervous system

A
  • Inflammation and damage

- Potential for auto-immune response

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6
Q

Explain how a toxin or drug may cause pathology of the nervous system

A
  • Block signalling
  • Damage specific cells
  • Toxicoinfectious deliver involving infection
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7
Q

Explain how toxicoinfectious delivery may occur

A
  • Toxins must pass through barriers or be released near site of action
  • Species differences in susceptibility
  • e.g. If receptors present on gut wall, toxin may bind to cell wall, but if not present may pass through the wall and target internal site
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8
Q

Describe the normal microbiology of the CNS

A
  • CNS sterile
  • To cause disease, organisms, toxins or drugs need to enter CNS
  • BBB effective so incidence of infection is low
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9
Q

What are the different pathways of breach of the BBB?

A
  • Transcellular (through the cell)
  • Paracellular (breaking of endothelial bonds and passage between cells)
  • Intracellular: use of other cells in order to get into the neuro tissue
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10
Q

Give an example of intracellular breach of the BBB and what this means for treatment

A
  • Listeria
  • Uses leukocytes as a route through neuro tissue
  • No damage to BBB
  • Higher concentration of antibiotics required to treat
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11
Q

How can infection of the CNS be detected?

A
  • Clinical signs
  • Physical effects
  • Imaging
  • Samples
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12
Q

List the clinical signs of CNS infection

A
  • Depression
  • Pyrexia
  • Cervical pain
  • Hyperaesthesia
  • Photophobia
  • Generalised rigidity
  • Seizures
  • Paralysis (local and general)
  • Ataxia
  • Papilloedema
  • Possible ophthalmic inflammation
  • Systemic signs e.g. septic shock, bradycardia
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13
Q

List the parameters within CSF that can be assessed with regards to infection of the nervous system, and give examples of what changes may indicate

A
  • Glucose (measured as % of blood glucose, reduced in meningitis)
  • Specific gravity (increased with cell proteins)
  • Intracranial pressure
  • Immunology (antibody titres to agents and cytology)
  • Microbiology (staining)
  • Enzyme analysis for cell breakdown (but not necessarily duet= to infection)
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14
Q

What would a CSF sample with RBCs present but clear supernatant indicate?

A

Iatrogenic contamination of sample

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15
Q

What would a CSF sample with RBCs present and erythophagocytosis or crenated RBCs indicate?

A

Intrathecal haemorrhage

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16
Q

What would a CSF sampe with elevated monomuclear pleocytosis indicate?

A

Viral and immune mediate disorders

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17
Q

What would a CSF sample with neutrophilic pleocytosis and healthy neutrophils indicate?

A

Necrotic CNS tumours or immune-mediated disease

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18
Q

What would a CSF sample with neutrophilic pleocytosis of degenerative/toxic neutrophils indicate?

A
  • Bacterial meningitis
  • Abscess
  • Necrotic CNS tumours
  • Cellular degeneration due to poor sample handling
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19
Q

What would a CSF sample with eosinophilic pleocytosis indicate?

A

Parasitic/fungal/protozoal diseases or eosinophilic meningoencephalomyelitis

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20
Q

What would a CSF sample with elevated lymphoblasts indicate?

A

CNS lymphoma

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21
Q

List the microbial tests that can be used in the investigation of neurological infectious diseases

A
  • Gram stain on CSF smears
  • Culture and sensitivity assays
  • Antigen tests on CSF fluid
  • ELISA for pathogen/toxin
  • Molecular tests e.g. PCR
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22
Q

Identify the common underlying causes of meningitis and encephalitis

A
  • Direct extensions from sinusitis,otitis media or interna, vertebral osteomyelitis and discospondylitis
  • Which can be secondary events to migrating grass awns, other foreign bodies, deep bite wounds, iatrogenic infections
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23
Q

List the common aerobic bacteria in the dog that cause neurological disease

A
  • Pasteurella multocida
  • Staphylococcus spp.
  • E. coli spp.
  • Streptococcus spp.
  • Actinomyces spp.
  • Nocardia spp.
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24
Q

List the common anaerobic bacteria in the dog that cause neurological disease

A
  • Bacteroides spp.
  • Peptostreptococcus anaerobicus
  • Fusobacterium spp.
  • Eubacterium spp.
  • Propionbacterium spp.
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25
Q

What are common sources of nervous system infection in the dog?

A

Endocarditis and septicaemia

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26
Q

Describe the prognosis for bacterial infection of the nervous system in dogs

A

Guarded even with treatment, relapse common and prolonged therapy may be required

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27
Q

Outline the treatment of bacterial meningitis or encephalitis in the dog

A
  • Appropriate use of antibiotics according to culture and serology results
  • Selection of broad spec antibiotics thaat can penetrate BBB e.g. ampicillin, metronidazole, tetracyclines, trimethoprim-sulfates, fluoroquinoles, 3rd gen cephalosporins
  • Bacteriocidal where possible
  • May need higher dose if BBB still in tact
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28
Q

Describe streptococcal meningitis in pigs (pathogen, conditions, epidemiology, prognosis)

A
  • Streptococcus suis
  • Meningitis, arthritis septicaemia, bronchopneumonia
  • Systemic disease that gets into the brain
  • Disease outbreak common in intensively reared
  • Meningitis often fatal, characterised by fever
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29
Q

Describe bastard strangles

A
  • Streptococcus equi
  • Extension of upper resp. tract and lymphatic infection that leads to abscessation in many organs incl. nervous tissue
  • ~ 1% strangles
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30
Q

How does discospondylitis commonly develop?

A

Bacteraemia, which may be from septic foci in other systems and may be a result of some clinical procedures such as surgery, dental work

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31
Q

List fungal agents that may cause discospondylitis in dogs and indicate the prevalence

A
  • Less frequent than bacterial cause
  • Aspergillus spp (most common)
  • Paecilomyces varioti
  • Mucor spp.
  • Fusarium spp.
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32
Q

Explain how bacteria can accumulate in the blood vessels of the vertebrae

A
  • In metaphysis (young)/epiphysis (adult) arterial capillaries form narrow loop with concavity directed towards feeding artery
  • Narrow loop, sudden change in diameter from fine arterial capillary to large venous sinus leads to slowed blood flow and increased turbulence
  • Microogranisms accumulate in efferent loop, aided by reduced concentration of phagocytic cells here
  • Followed by initial inflammatory reaction leading to formation of microthrombus
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33
Q

Describe the pathogenesis of bacterial discospondylitis following the establishment of infection

A
  • Tissue necrosis and bone destruction
  • Perpetuated by:
    1: Mutliplication of pathogen
    2: Lytic nature that exudate acquires due to elevated local lysosomal activity
    3: Ischaemic damage due to accumulation of exudate in rigid structure
    4: Subarachnoid abscess in some cases
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34
Q

What is the consequence of host defences responding to devitalised tissue in discospondylitis?

A

Tissue becomes surrounded by granulation tissue

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35
Q

Following the initial bone destruction in discospondylitis, how does the disease progress?

A
  • Invasion of subchondral bone tissue and eventually the intervertebral disc
  • Accumulate exudate may diffuse to veretbral canal or paravertebral soft tissue, destroying osteocytes and vascular structures
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36
Q

How may the propagation of the infection in discospondylitis affect the spinal cord?

A
  • By the action of the exudate
  • By the growth of granulation tissue
  • Potential for spinal compression
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37
Q

What approach should be taken if there is no response to appropriate antibacterial treatment for discospondylitis?

A
  • Reconsider diagnosis, consider aspergillosis for example

- If no response to treatment after that, surgery

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38
Q

Describe the properties of Listeria monocytogenes (appearance, growth conditions, metabolic activity)

A
  • Gram +ve rod
  • grow on non-enriched media
  • Tolerate wide range of pH and temperatures
  • Small haemolytic colonies on BA
  • Facultative anaerobes, catalase positive, oxidase negative
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39
Q

Describe the pathogenesis of infection with Listeria monocytogenes

A
  • Contaminated feed
  • Possible septicaemia, encephalitis, abortion, sepsis, meningitis
  • Meningitis often complicated by encephalitis
  • Ocular infections common
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40
Q

Describe the neurotropic spread of Listeria monocytogenes

A
  • Enters mammalian cells via induced phagocytosis
  • Can escape vacuole
  • Propel self using actin polymerisation
  • Spread from cell to cell
  • Can ascend nervous tissue from oral cavity infection to CNS
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41
Q

Outline the clinical signs of Listeria monocytogenes

A
  • Characteristic neurological signs, abortion
  • Dullness, circling, tilting of head, facial paralysis
  • Unilateral facial paralysis resulting in drooling, dropping of eyelids and ears
  • In ruminants: encephalititis, abortion, septicaemia, endophthalmitis
42
Q

What is the incubation period for neural listeriosis?

A

14-40 days

43
Q

Identify potential diagnostic specimens for Listeria monocytogenes in the following scenarios

a: neurological signs
b: abortion
c: septicaemia

A

a: CSF fluid from medulla or pons
b: cotyledons, foetal abomasal/uterine discharge
c: fresh liver, spleen or blood

44
Q

Describe the potential findings in diagnostic samples positive for Listeria monocytogenes

A
  • Smears: G+ve rods
  • Immunofluorescence
  • Histologically may see microabscesses and heavy perivascular mononuclear cuffing
  • White cell numbers ?1.2x10^7
45
Q

Outline the prevention for Listeria monocytogenes

A
  • Vaccines ineffective
  • Feed method that reduces ocular contact
  • Ensure good quality silage fed
46
Q

Give examples of toxin producing bacteria

A
  • Clostridium tetani (tetanus)
  • Clostridium botulinum (botulism)
  • E. coli (oedema disease)
47
Q

Give an example of a toxin that is produced symbiotically on pasture

A

Acremonium loliae fungal endophyte, leads to rye grass staggers, sporadic in UK

48
Q

Give the organism, toxin effect and species affected by focal symmetrical encephalomalacia

A
  • Clostridium perfringes type D
  • Causes vasculopathy, encephalomalaxcia
  • Affects sheep/lambs and goats
49
Q

Describe the sampling requirements for the diagnosis of clostridial infection

A
  • Fastidious anaerobes, samples must be kept anaerobic
  • samples must be from live/recently dead animals as Clostridia increase in putrifying body
  • Culture promptly under anaerobic conditions
  • Wear gloves, toxins potent
  • Blood culture not performed generally
50
Q

Describe the morphology of Clostridia

A
  • Drumstick appearance
  • All form endospores
  • G+ve rods, relatively large
51
Q

Compare C. tetani and C. botulinum based on:

a: the site of toxin production
b: genes that regulate the production
c: antigenic type
d: mode of action of toxin

A

a: T: in wounds, B: in carcasses, decaying veg, canned foods, can be toxicoinfectious
b: T: on plasmids, B: usually genome
c: T: one type, tetanospasmin, B: 8 distinct types A to G
d: T: synaptic inhibition, B: inhibition of neuromuscular junction

52
Q

How are C tetani and C botulinum generally differentiated from one another?

A
  • Colonial morphology
  • Biochemistry
  • Toxin identification
  • Molecular tests
53
Q

Describe toxicoinfectious botulism

A
  • IN horse, Clostridium grows in GIT and produces toxin in vivo = shaker foal in USA
  • Can colonise in wounds and produce toxin
54
Q

Which antigenic types of botulinum toxin cause the most outbreaks in domestic animals?

A

Ca/b and D

55
Q

Outline the treatment and control of botulism

A
  • Antitoxins available, neutralise circulating toxins but not effective once toxin enters nerve terminal
  • Guanidine ydrochloride to enhance neurotransmitter release
  • Vaccine available for horses and cattle in endemic areas
  • removal of suspect food stuff
56
Q

Describe the mechanism of action of the botulinum toxin

A
  • Acts at NMJ
  • Stops stimulation and leads to flaccid paralysis, toxin absorbed from GIT
  • Circulates blood
  • Acts at NMJs of cholinergic nerves and peripheral autonomic nerve synapses
  • Binds somatic and autonomic nerve terminals
  • Inhibits neurotransmitter release
  • Death from paralysis of respiratory muscles
57
Q

Describe the mechanisms of action of the tetanus toxin

A
  • Blocks inhibitor neurotransmitter release triggering spastic paralysis
  • Binds ganglioside receptors on motor neurones
  • Then moves into vesicles via axonal transport to nerve body and dendritic processes
  • Toxin then transfers trans-synaptically to inhibitory neurones where it interacts with and blocks vesicle docking and inhibitory NT release is blocked
58
Q

What is the incubation period for tetanus?

A

5-10 days

59
Q

Describe the clinical signs of tetanus

A
  • Stiffness
  • Local spasms
  • effects on heart and resp rate
  • dysphagia
  • Altered facial expression
60
Q

Outline the diagnosis of tetanus

A
  • Usually presumptive based on clinical signs
  • Differentiate from strychnine poisoning
  • Gram smears, look for characteristic drumstick forms of C tetani
61
Q

Describe the treatment of tetanus

A
  • Antitoxin administration
  • Large doses of penicillin IM
  • Debridement of wounds (potentially use hydrogen peroxide wash)
62
Q

Outline the control options for tetanus

A
  • Vaccination of at risk animals (common)
  • Debridement of wounds
  • Passive antitoxin in unvaccinated animals
63
Q

How long is the incubation period for botulism?

A

3-17 days after ingestion

64
Q

Describe the clinical signs of botulism

A
  • Dilated pupils
  • Dry mucous membranes
  • Decreased salivation
  • Tongue flaccidity
  • Dysphagia
65
Q

Outline the diagnosis of botulism

A
  • Mainly based on clinical signs and food intake history

- Confirmation by detection of toxin in serum (not confirmed method)

66
Q

List some viral infections that may cause neurological signs in small animals

A
  • Pestiviruses
  • Feline infectious peritonitis (FIP)
  • Canine distemper
  • Borna virus
  • Tick borne encephalitides
  • Schmallenberg virus
67
Q

What are the 3 categories of viruses that cause neurological signs

A
  • Those causing signs in neonate following infection in utero
  • Viruses causing PREDOMINANTLY neurological signs
  • Viruses that MAY cause neurological signs
68
Q

List the viruses that cause neurological signs in neonates

A
  • Pestiviruses: BVD, Border disease, classical swine fever
  • Parvovirus: feline panleukopaenia
  • Bunyavirus: Schmallenberg virus
69
Q

What is required in order for a virus to be able to cause neurological signs in the neonate following infection in utero?

A
  • Dam must be susceptible to viral infection i.e. not vaccinated or previously exposed
  • Virus must be able to cross placenta once dam is infected
70
Q

Describe the neurological signs of BVD

A
  • Minor part of BVDV and variable
  • Recumbency
  • Ataxia
  • Blindness
  • Lack of coordination
  • Twtiching
  • Marked intention tremor
  • Signs vary depending on dose of infection and degree of response of foetus
71
Q

When does infection with BVDV need to take place in order to cause neurological signs in the neonate? Explain

A

~d100-200 of gestation - development of cerebellum is at maximum between d130 and 160

72
Q

Describe how the BVDV status of calves differs depending on when the infection occured

A
  • After d120, foetus can mount immune response
  • If before, is persistently infected and no immune response, can infect rest of herd
  • Most are antibody positive and have no carrier status
73
Q

What causes the neurological signs seen with in utero infection of BVDV?

A

Lack of cerebellum

74
Q

Describe the clinical appearance of Border disease

A
  • Early embryonic death
  • Abortion
  • Lambs with hairy fleece and involuntary tremor
75
Q

How does in utero infection with Border disease lead to the neurological clinical signs?

A

Virus causes demyelination of nerve fibres in CNS, impulse coordination impaired

76
Q

What is the consequence for animals infected with Border disease in utero?

A

Often persistently infected and need to be culled in order to prevent spread to rest of flock

77
Q

Describe how an animal becomes infected with parvovirus

A
  • Faecal oral transmission
  • Persists in environment for up to a year
  • Transmission by direct contact or fomites
  • Infects lymph nodes of naso- and oropharynx and then spreads to other tissues
78
Q

Describe the pathogenesis of parvovirus in cats

A
  • Panleukopaenia: decreased WBC count, killing of lymphoid and myeloid stem cells, high risk of secondary infection
  • Enteritis: killing of stem cells in crypts
  • Cerebellar hypoplasia: infection in neonatal kittens in utero within 2 weeks of birth leads to nervous signs
79
Q

Describe the presentation of kittens with in utero parvovirus infection

A

Control of coordination/balance lost

80
Q

Outline the treatment of feline parvovirus

A
  • Depends on severity of signs and how much owner is willing to do
  • Key part is treatment of secondary infection risk
81
Q

What virus is Schmallenberg and how is it transmitted?

A

Orthobunyavirus

- Transmitted by Culicoides mainly

82
Q

Describe the clinical signs of in utero Schmallenberg virus infection

A
  • Mainly stillbirths, abortion, congenital deformities
  • Unable to suck
  • Blindness
  • Ataxia
83
Q

Explain the pathogenesis of the neurological signs of an in utero Schmallenberg infection

A
  • Hydrancephaly: brain replaced by sac of fluid

- Poliomyelitis: inflammation of brain and spinal cord

84
Q

Give examples of viral diseases with primarily neurological signs

A
  • Borna disease

- Tick borne encaphlitides (Louping ill, Spanish sheep encephalitis, Turkish sheep encephalitis/Greek goat encephalitis)

85
Q

Which species are affected by Borna disease?

A
  • Horses
  • Cats
  • Sheep
  • Rabbits
  • Ostrich
  • Humans
86
Q

Describe the pathogenesis of Borna disease

A

Infects neurons, cellular immune response leads to tissue destruction causing meningitis, encephalomyelitis

87
Q

Describe the clinical signs of Borna disease

A
  • Pyrexia
  • Ataxia
  • Pharyngeal paralysis
  • Hyperaesthesia
  • Fatal within several weeks
88
Q

Describe the viral structure, and geographical locality of Borna disease

A
  • Enveloped -ve sense ssRNA virus

- Endemic in upper Rhine valley area of Germany

89
Q

Where do tick borne encephalitides mostly occur?

A

Upland, moorland areas with sparse grassland

90
Q

Describe the virus that causes tick borne encephalitides

A
  • Flaviviruses

- Enveloped +ve sense ssRNA virus

91
Q

Describe the transmission of Louping ill

A
  • Sheep-tick lifecycle
  • Ticks infected when feed on viraemic animal, o tick to tick spread
  • Virus replicates in gut and salivary glands of tick
  • Transtadial transmission within ticks
  • Bites and able to infect lots of hosts
92
Q

Describe infection and clinical signs of Louping ill

A
  • Typically lambs once MDA has waned after movement to upland pasture
  • Virus infects lymph nodes then spread to other lymphoid tissue +/- CNS
  • Neurological signs include tremors, exaggerated gait, death
93
Q

Outline how immunosuppression affects Louping ill and give common causes

A
  • Anaplasma phagocytophila (tick borne fever) worsens prognosis as it predisposes to secondary infections such as Staphylococcus aureus pyaemia
  • Anaplasma characterised by high fever, inclusions in circulating neutrophils, reduced milk yield, abortion, reduced fertility in rams
94
Q

Give examples of viruses that MAY cause neurological signs

A
  • Canine distemper

- Feline infectious peritonitis

95
Q

What is canine distemper?

A

Morbillivirus (Paramyxovirus)

96
Q

Which dogs are most susceptible to canine distemper?

A

Young dogs

97
Q

Describe infection with canine distemper

A
  • transmission by direct contact
  • Virus replicates in URT
  • Spread to tonsils/lymph nodes
  • Spills into blood stream leading to viraemia
  • Viraemia and systemic spread up to epithelia of CNS
98
Q

Describe the clinical signs of canine distemper

A
  • Pyrexia, depression
  • Ocular and nasal discharge
  • Cough
  • Vomiting and diarrhoea
  • Hyperkeratosis of nose/pads (hardpad)
99
Q

Outline the prognosis for canine distemper

A
  • Solid immune response = recovery
  • Poor immune response = neuro signs
  • Prognosis generally guarded
100
Q

Describe the treatment of canine distemper

A
  • supportive therapy and treatment for secondary infections with antibiotics
  • Fluid therapy, antibiotics
  • Anticonvulsant if mild CNS signs, if severe consider euthanasia
  • Interferon omega may work but not licensed, little evidence
  • Rely on immune response of animal for recovery

NEU2 (23 decks)

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